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PubMed1982

Na+/H+ antiporter of brush border vesicles: studies with acridine orange uptake.

Fluorescence quenching of acridine orange was used to characterize the generation and collapse of pH gradients by the Na+/H+ antiporter of brush border membrane vesicles prepared from rabbit renal cortex. Quenching was observed when acridine orange, a weak base, was taken up to an acidic intravesicular space. Na+/H+ exchange was examined with both Na+ uptake and efflux studies. Acridine orange fluorescence quenching demonstrated the cation specificity of the Na+/H+ antiporter (i.e., sodium and lithium) and was inhibited by amiloride. Parallel studies with nigericin, a K+/H+ antiporter, demonstrated that acridine orange responded very rapidly to pH gradients. Therefore, acridine orange equilibration was not rate limiting in our studies of the Na+/H+ antiporter. Initial rate measurements were made to obtain kinetic parameters for the Na+/H+ antiporter. In sodium influx studies, the half-maximal rate of acridine orange fluorescence change was obtained with an external sodium concentration of 13.3 +/- 0.5 mM.

Acridine Orange↗
PubMed1986

The mobility of intramembrane particles in non-haemolysed human erythrocytes. Factors affecting acridine-orange-induced particle aggregation.

It has previously been shown that reversible intramembrane particle aggregation can be induced in non-haemolysed human erythrocytes. This phenomenon, which can be induced by the cationic dye Acridine Orange, has been further investigated using different experimental conditions that are expected to influence the rate of aggregation of the particles. In addition to the concentration of the dye, the rate of aggregation was also found to be dependent on the extracellular and intracellular pH, as well as on the type of buffer used. While lowering the pH of the Acridine Orange solutions resulted in decreased particle clustering, low intracellular pH increased and elevated intracellular pH decreased particle aggregation. Furthermore, at a given dye concentration and a given pH, Acridine Orange caused more intense aggregation in Tris-buffered saline than in isotonic phosphate buffer or phosphate-buffered saline. Under appropriate conditions Acridine Orange caused significant particle aggregation at concentrations as low as 0.25 mM within 30 s. During this period only discocyte-stomatocyte transformation occurred; neither agglutination nor vesiculation of the erythrocytes could be detected. Treatment of the erythrocytes with Diamide (Serva), which cross-links spectrin via disulphide bridges and thereby reduces lateral diffusion of integral membrane proteins over large distances, had no inhibitory effect on Acridine-Orange-induced particle aggregation. Heating the erythrocytes to 50 degrees C, at which temperature denaturation of spectrin and fragmentation of the erythrocytes occur, and subsequently incubating them in Acridine Orange at room temperature, caused an almost maximal rate of particle aggregation within 10-30 s, without haemolysis. The possible mechanism and significance of the particle aggregation phenomenon are discussed.

Acridine Orange↗
PubMed2005

Synthesis and cytotoxic activity of acronycine analogues in the benzo[c]pyrano[3,2-h]acridin-7-one and naphtho[1,2-b][1,7] and [1,10]-phenanthrolin-7(14H)-one series.

Condensation of 1-bromo-2-naphthalenecarboxylic acid (9) with 7-methoxy-2,2-dimethyl-2H-1-benzopyran-5-ylamine (13) followed by acid-mediated cyclization afforded 6-methoxy-3,3-dimethyl-3,14-dihydro-7H-benzo[c]pyrano[3,2-h]acridin-7-one (15), which was further methylated into 6-methoxy-3,3,14-trimethyl-3,14-dihydro-7H-benzo[c]pyrano[3,2-h]acridin-7-one (benzo[c]acronycine) (3) and 6,7-dimethoxy-3,3-dimethyl-3H-benzo[c]pyrano[3,2-h]acridine (4). Osmium tetroxide oxidation of 15 gave the (+/-)-cis-diol 16, which afforded the benzopyranoacridine and benzopyranoacridone esters 17-22 upon acylation. Condensation of 9 with suitable aminoquinolines 23-25 afforded the carboxylic naphthylquinolylamines 26-28. Cyclization gave the corresponding naphtho[1,2-b][1,10]-phenanthrolin-7(14H)-ones 29 and 30, and naphtho[1,2-b][1,7]-phenanthrolin-7(14H)-one 31, which were subsequently N-methylated to the desired 14-methylnaphtho[1,2-b][1,10] and [1,7]-phenanthrolinones 6, 7, and 8. Benzo[c]pyrano[3,2-h]acridin-7-one derivatives 3, 16, and 22 displayed cytotoxic activities within the same range of magnitude as acronycine itself, whereas 7-alkoxybenzo[c]pyrano[3,2-h]acridine and 7-acyloxybenzo[c]pyrano[3,2-h]acridine derivatives 4 and 17-21 were less active when tested against L1210 murine leukemia cells in vitro. Naphthophenanthrolinones 6-8 were devoid of significant antiproliferative activity, but compounds 29-31 bearing no substituent on the nitrogen atom at position 14 were more potent.

Acridines↗
PubMed2001

Interest of acridine derivatives in the anticancer chemotherapy.

DNA is considered as one of the main targets for anticancer drug design. The planar structure of acridines confers to the molecules the ability to bind DNA by intercalation and therefore to interfere with metabolic processes. A large number of natural alkaloids and synthetic acridine derivatives have been tested as anticancer agents. So far, a few molecules have entered clinical trials and have been approved for chemotherapy. The mechanisms of action are not fully understood. Cytotoxicity may be related to potent enzyme inhibition. Topoisomerase and telomerase activities may be strongly affected by acridines. The affinity of acridines for DNA has also been used to design new active compounds in which a DNA modifying group is tethered to the acridine nucleus. Acridine derivatives display other pharmacological properties such as antibacterial and antimalarial activities. They are also tested for Alzheimer's disease.

Acridines↗
PubMed1994

Acridine orange diagnosis of Plasmodium falciparum: evaluation after experimental infection.

The value and role of the acridine orange/microhematocrit tube method (quantitative buffy coat [QBC] analysis) in the diagnosis of malaria remains controversial. To establish the true sensitivity of this test in comparison with the thick blood film, we studied 49 subjects who were experimentally infected with Plasmodium falciparum in 10 malaria vaccine and infectivity trials. Diagnosis was made by the acridine orange staining method 1-3 days earlier than by the thick blood film in 23 subjects (47%) and at the same time as the thick blood film in 20. On the other hand, diagnosis was made by thick blood film earlier than by the acridine orange staining method in six individuals. There were no false positive results using acridine orange among 584 specimens studied. Diagnosis was made using acridine orange at a parasitemia of less than 11 parasites/microliters of blood in 65% of cases. Where available, the acridine orange assay is clearly preferable in terms of speed and accuracy to the thick blood film for diagnosis with parasitemias of less than 150/microliters of blood, and perhaps as important, for ruling out infection with P. falciparum in a symptomatic patient.

Acridine Orange↗
PubMed1990

Acridine orange and Gram stains in infectious keratitis.

Two hundred thirty consecutive cases of presumed infectious keratitis were reviewed. Cultures were positive in 49.5% (114 of 230). Acridine orange stain sensitivity (81%) was significantly greater than gram stain sensitivity (65%) (p less than 0.002). Gram stain specificity was 92%, and acridine orange specificity was 89%. In keratitis with low or moderate growth, acridine orange was positive in 73% (61 of 84) as compared with Gram stain 53% (45 of 84), (p less than 0.001). In cases of heavy microbial growth, Gram stain was positive in 97% (29 of 30), acridine orange in 100% (30 of 30). This study demonstrates that both Gram stain and acridine orange stain are excellent in cases of infectious keratitis with heavy microbial growth, but that acridine orange is significantly better than Gram stain in cases with low amounts of organisms.

Acridine Orange↗
PubMed1990

A further characterization of acridine-photosensitized inhibition of mast cell degranulation.

The purpose of this study was to further characterize acridine-photosensitized inhibition of mast cell degranulation. Acridine plus UVA radiation (320-400 nm) inhibited degranulation in response to antigen in IgE-sensitized rat serosal mast cells and in response to concanavalin A, which acts by a mechanism similar to antigen-IgE challenge. Removing oxygen from the incubation medium prevented the acridine-photosensitized inhibition of mast cell degranulation in response to 48/80. Acridine plus UVA radiation did not decrease mast cell ATP content, thus excluding inhibition of ATP production as a mechanism for photosensitized inhibition of mast cell degranulation. Although the viability of mast cells, as determined by uptake of trypan blue, was not affected 3 h after treatment with acridine plus UVA radiation, viability decreased by 6 h, and by 22 h 44% of the cells were nonviable. These results indicate that degranulation of mast cells by a variety of agents is inhibited by UVA plus acridine treatment, and that photosensitization requires oxygen and occurs before cytotoxicity.

Acridines↗
PubMed1986

Bacterial and mammalian cell mutagenicity of four optically active bay-region 3,4-diol-1,2-epoxides and other derivatives of the nitrogen heterocycle dibenz[c,h]acridine.

The mutagenic activities of the enantiomers of the diastereomeric pair of bay-region 3,4-diol-1,2-epoxides of the nitrogen heterocycle, dibenz[c,h]acridine, have been evaluated in histidine-dependent strains of Salmonella typhimurium and in an 8-azaguanine-sensitive line of Chinese hamster cells. In strains TA 98 and TA 100 of S. typhimurium the pair of enantiomers with [1R,2S,3S,4R] and [1S,2R,3R,4S] absolute configuration and the benzylic hydroxyl group trans to the epoxide oxygen are 2 to 4 times more mutagenic than the [1S,2R,3S,4R] and [1R,2S,3R,4S] isomers in which the benzylic hydroxyl and epoxide oxygen are cis. In both strains of bacteria there is very little difference in mutagenic activity between the enantiomers of each diastereomer. In contrast to these results in bacteria, the bay-region 3,4-diol-1,2-epoxide isomer with [1R,2S,3S,4R] absolute configuration is 5 to 7 times more mutagenic to Chinese hamster V79 cells than are the other 3 isomers. The enantiomeric pair of bay-region tetrahydro-1,2-epoxides of dibenz[c,h]acridine are at least 7 times more mutagenic than the diol-epoxides in the Salmonella assay, and no difference in mutagenic activity is observed between enantiomers. In the Chinese hamster V79 cell system, however, the tetrahydro-1,2-epoxide with [1R,2S] absolute configuration is 2- to 3-fold more mutagenic than its enantiomer with [1S,2R] absolute configuration. Homogeneous rat liver epoxide hydrolase does not catalyze the hydration of the diol-epoxide isomers to nonmutagenic products, although the tetrahydroepoxides, especially the tetrahydro-3,4-epoxide, are metabolized by the enzyme. Results of metabolic activation experiments with the bacterial mutagenesis system and microsomes from Aroclor 1254-treated rats are consistent with the mutagenicity data described above and support the concept that dibenz[c,h]acridine is metabolically activated to a bay-region diol-epoxide. Notably: (a) 3,4-dihydrodibenz[c,h]acridine, the expected precursor of a bay-region tetrahydroepoxide, is metabolized to a potent mutagen; (b) racemic dibenz[c,h]acridine 3,4-dihydrodiol is metabolized to products which are several-fold more mutagenic than are products of the metabolism of dibenz[c,h]acridine or its 1,2- or 5,6-dihydrodiols; and (c) the tetrahydro-3,4-diol, which lacks the isolated bay-region double bond, is not metabolically activated to a bacterial mutagen.

Acridines↗
PubMed1978

A comparison of acridine orange and Feulgen cytochemistry of human tumor cell nuclei.

Specimens of cells derived from tumors of the human female genital tract plus normal cells as standards have been divided into aliquots and stained according to acridine orange or pararosanilin:Feulgen procedures. Acridine orange-stained cells were slit-scanned for 535 nm nuclear fluorescence; Feulgen-stained cells were comb-scanned for 580 nm nuclear absorbance. For each specimen examined, the tumor cell:normal cell ratio of mean nuclear fluorescence following acridine orange staining was greater than the tumor cell:normal cell ratio of mean nuclear absorbance following Feulgen staining. The tumor cell:normal cell ratio of mean nuclear fluorescence ranged from 2.3 for a nonkeratinizing squamous cell carcinoma to 3.9 for a keratinizing squamous cell carcinoma. The tumor cell:normal cell ratio of mean nuclear absorbance ranged from 1.4 for a mixed mesodermal sarcoma to 2.3 for a small cell squamous cell carcinoma. These results indicate that the elevated nuclear fluorescence intensity from acridine orange-stained tumor cells cannot be explained solely on the basis of elevated Feulgen:DNA content. An alternative hypothesis, consistent with these results, is that DNA is the principal binding substrate for intranuclear acridine orange and that the DNA of certain tumor cells is more accessible to acridine orange than is the DNA of normal cells.

Acridines↗
PubMed1979

Staining of DNA-phosphate groups with a mixture of azure A and acridine yellow.

This paper deals with staining of DNA-phosphate groups with a mixture of an equal parts of aqueous solution of azure A and acridine yellow in a 1:1 proportion and also embodies a study of the absorption properties of the stained nuclei. It also embodies results of sequential staining of nuclei stained first with azure A followed by staining with acridine yellow and vice versa, after extraction of RNA with cold phosphoric acid. The results indicate that the absorption peaks of nuclei differ from those of nuclei stained for DNA-aldehyde molecules with azure A-SO2 or acridine yellow-SO2. The in vitro absorption characteristics of an aqueous solution of azure A and those of an aqueous solution of acridine yellow are also presented herein. The conclusion obtained from this study is that all the phosphate groups of DNA do not take part in the staining process when staining is carried out with azure A or acridine yellow alone after after RNA has been extracted. This is because the nuclei stained with these dyes sequentially show the presence of acridine yellow-DNA and azure A-DNA complex.

Acridines↗
PubMed2000

Complexes of acridine and 9-chloroacridine with I2: formation of unusual I6 chains through charge-transfer interactions involving amphoteric I2.

Acridine and 9-chloroacridine form charge-transfer complexes with iodine in which the nitrogen-bound I2 molecule is amphoteric; one end serves as a Lewis acid to the heterocyclic donor, while the other end acts as a Lewis base to a second I2 molecule that bridges two acridine.I2 units. In the acridine derivative [(acridine.I2)2.I2, 1], the dimer has a "zigzag" conformation, while in the 9-chloroacridine derivative [(9-Cl-acridine.I2)2.I2, 2], the dimer is "C-shaped". The thermal decomposition of the two complexes is very different. Compound 1 loses one molecule of I2 to form an acridine.I2 intermediate, which has not been isolated. Further decomposition gives acridine as the form II polymorph, exclusively. Decomposition of 2 involves the loss of two molecules of I2 to form a relatively stable intermediate [(9-Cl-acridine)2.I2, 3]. Compound 3 consists of two 9-Cl-acridine molecules bridged through N...I charge-transfer interactions by a single I2 molecule. This compound represents the first known example, in which both ends of an I2 molecule form interactions in a complex that is not stabilized by the extended interactions of an infinite chain structure. The ability of the terminal iodine of an N-bound I2 to act either as an electron donor (complexes 1 and 2) or as an electron acceptor (complex 3) can be understood through a quantum mechanical analysis of the systems. Both electrostatic interactions and the overlap of frontier molecular orbitals contribute to the observed behavior.

Journal Article↗
PubMed2002

Antioxidant and lysosomotropic properties of acridine-propranolol: protection against oxidative endothelial cell injury.

The antioxidant and lysosomotropic properties of a fluorescent analogue of propranolol, 9-amino-acridine-propranolol (9-AAP) were compared to those of propranolol. Using isolated microsomal membranes exposed to a superoxide and hydroxyl radical generating system, 9-AAP was found to be at least 10-fold more potent than propranolol (and about 50% as potent as vitamin E) in inhibiting lipid peroxidation. In cultured endothelial cells, 9-AAP afforded moderate protective effect against acute loss of glutathione but potent cytoprotective activity against free radical-mediated loss of viability/survival. Intracellular localization of 9-AAP was examined by fluorescent microscopy and compared with two known fluorescent lysosomal markers: acridine orange and Lysosensor. All three agents appeared to localize to similar peri-nuclear vesicles, presumably lysosomes or pre-lysosomes. Lysosensor fluorescence was not observable in the presence of 9-AAP, foreclosing the possibility of a direct dual labeling experiment. We employed the pH sensitivity of acridine orange to determine if it labels the same vesicles as 9-AAP. When the endothelial cells were preloaded with acridine orange, washed and resuspended in buffer containing 9-AAP, the dark orange-labeled vesicles observed with acridine orange alone became increasingly lighter with time. Since the fluorescence of acridine orange is altered by pH change, this spectral shift in fluorescence emission is consistent with the indication that added propranolol (or the analog) leads to lysosomal alkalization. In conclusion, 9-AAP is both a strong antioxidant and a lysosomotropic agent that is remarkably insensitive to photobleaching. These properties may contribute to the enhanced endothelial cytoprotective effects against free radical-induced injury.

Animals↗
PubMed1985

Proton and phosphorus nuclear magnetic resonance studies of an oligothymidylate covalently linked to an acridine derivative and of its binding to complementary sequences.

An oligodeoxynucleotide containing four thymines and covalently attached to an acridine derivative through its 3'-phosphate [(Tp)4(CH2)5Acr] was synthesized. Its conformation in solution was investigated by proton magnetic resonance. Both intramolecular interactions between the acridine dye and thymines and intermolecular interactions were demonstrated. Both proton and phosphorus magnetic resonances were used to study the specific interaction of (Tp)4(CH2)5Acr with poly(rA) and (Ap)3A. The results were compared to those obtained when the acridine-containing substituent was replaced by an ethyl group attached to the 3'-phosphate of the oligothymidylate. The acridine dye strongly stabilized the complexes formed with both poly(rA) and (Ap)3A. Upfield shifts of both adenine and acridine proton resonances were observed in the complexes. These results were ascribed to an intercalation of the acridine ring between A X T base pairs of the duplex structure formed by the oligothymidylate with its complementary oligoadenylate sequence. An analysis of proton and phosphorus chemical shifts as well as measurements of T1 relaxation times at different temperatures allowed us to propose several structures for the complexes formed by (Tp)4(CH2)5Acr with its complementary sequence.

Adenine Nucleotides↗
PubMed1996

Coordination and peri-Carbon Metalation of 1-Nitro-9-[(2-aminoethyl)amino]acridines toward Platinum(II). Evidences for Hydrogen Bonding between Endocyclic N(10)H and Chloride Ion.

The antitumor drugs 1-nitro-9-[(2-(dialkylamino)ethyl)amino]acridines (alkyl = Me, A(1); Et, A(2)) with platinum(II) give tridentate coordination compounds in which the two nitrogens of the ethylenediamine side chain and the C(8) carbon atom of the acridine ring system act as donor atoms. An excess of triphenylphosphine displaces the residual chloride coordinated to platinum but leaves unaltered the tridentate acridine ligand. The structures of [Pt(A(1)-H)Cl], 1, and [Pt(A(1)-H)(PPh(3))]Cl, 3, have been solved by single-crystal X-ray diffraction. 1.CHCl(3) crystallizes in the orthorhombic system, space group P2(1)2(1)2(1) (no. 19), with a = 8.715(1) Å, b = 11.045(2) Å, c = 22.609(4) Å, Z = 4, R = 0.0559, and R(w) = 0.0561 for 1502 reflections with F > 3sigma(F). 3.(1)/(2)CH(2)Cl(2) crystallizes in the monoclinic system, space group P2(1)/c (no. 14), with a = 13.418(3) Å, b = 14.053(3) Å, c = 18.918(4) Å, beta = 97.21(3) degrees, Z = 4, R = 0.0591, and R(w) = 0.0611 for 3608 reflections with F > 4sigma(F). In both complexes the acridine ligand adopts an imino-type configuration with the proton of the exocyclic 9-amino group shifted on N(10). Because of a severe steric interaction between the nitro group in the 1-position and the chelate diamine chain in the 9-position, the acridine moiety is folded about the C(9)-N(10) vector with an average angle between outer rings of 12 degrees. Moreover, the acridine aromatic moiety and the platinum coordination planes are twisted, forming a dihedral angle of ca. 20 degrees. The steric repulsion between the nitro and the diamine groups appears to provide the driving force to metalation. The H(10) proton has a great tendency to be engaged in H-bonding as shown by X-ray and solution studies. The formation of a H-bond with a rather poor acceptor such as the chloride ion can cause a downfield shift of the H-resonance as large as 6 ppm.

Journal Article↗
PubMed1988

The induction of chromosomal aberrations and SCE by visible light in combination with dyes. I. The effect of hypoxia during light exposure in unsynchronized Chinese hamster ovary cells, sensitized with acridines.

A comparison has been made between the ability of different acridine compounds to act as sensitizers for visible light (400-700 nm) induced chromosomal aberrations and sister-chromatid exchanges (SCE) in unsynchronized Chinese hamster ovary (CHO) cells. Cells were treated for 20 min with acridines (0.1-5.0 microgram/ml), washed free of excess dye and subsequently exposed to visible light (2 x 40 W/8 W m-2) either in air or in nitrogen for 5-15 min. The 4 acridines tested, proved to be effective sensitizers for the induction of both chromosomal aberrations and SCE by visible light. The most pronounced effect was observed when the light exposure of the fluorochrome-pretreated cells was performed in air. Hypoxic conditions during light exposure reduced the effect dramatically, especially in the case of induced chromosomal aberrations. The order of efficiency for the induction of both chromosomal aberrations and SCE was acridine orange greater than acridine yellow greater than proflavine greater than 3,6-diamino-10-methylacridine. The results are discussed in terms of S-independent versus S-dependent mechanisms for inducing chromosomal alterations and the potential involvement of oxygen-derived free radicals in this process.

Acridine Orange↗
PubMed2003

Frameshift mutations induced by three classes of acridines in the lacZ reversion assay in Escherichia coli: potency of responses and relationship to slipped mispairing models.

The frameshift mutagenicity of 9-aminoacridine (9AA) was compared with that of quinacrine, the acridine mustards ICR-191 and quinacrine mustard (QM), and the nitroacridine Entozon in the lacZ reversion assay in Escherichia coli. As intercalating agents, 9AA and quinacrine cause mutations through noncovalent associations with DNA. Mustards and nitroacridines form covalent adducts in DNA and give rise to different spectra of mutations. Quinacrine and 9AA most effectively induced -1 frameshifts in a run of guanine residues, with 9AA being the more potent mutagen. They also induced +G frameshifts. The acridine mustard ICR-191 was a stronger mutagen than 9AA, owing largely to its potent induction of +G frameshifts. QM induced +G frameshifts more strongly than did its nonreactive counterpart quinacrine. The nitroacridine Entozon differed from the other acridines in being a potent inducer of -2 frameshifts, but it was less effective in inducing +/-1 frameshifts. Quinacrine, although a simple intercalator, induced all five kinds of frameshift mutations detected in the assay, as did the acridine mustards. Although +A and -A frameshifts were induced, adenine runs were less susceptible to acridine mutagenesis than guanine runs. The patterns of frameshift mutagenicity in the lacZ assay are similar to those in an assay based on the reversion of mutations in the tetracycline-resistance gene of the plasmid pBR322. The similarity suggests that the responses reflect the inherent bacterial mutagenicity of the compounds in the local sequence context and are not highly dependent on the broader sequence context. The results are interpreted with respect to slipped mispairing models of frameshift mutagenesis.

Acridines↗
PubMed2003

Classification of larval circulating hemocytes of the silkworm, Bombyx mori, by acridine orange and propidium iodide staining.

Circulating hemocytes of the silkworm can be classified by fluorescence microscopy following staining with acridine orange and propidium iodide. Based on their fluorescence characteristics, three groups of circulating hemocytes can be distinguished. The first group, granulocytes and spherulocytes, is positive for acridine orange and contain bright green fluorescent granules when observed by fluorescence microscopy. In granulocytes, these green granules are heterogeneous and relatively small. In contrast, in spherulocytes, the green granules appear more homogenous and larger. The second group of hemocytes consists of prohemocytes and plasmatocytes. These cells appear faint green following staining with acridine orange and do not contain any green fluorescent granules in the cytoplasm. Prohemocytes are round, and their nuclei are dark and clear within a background of faint green fluorescence. Inside the nucleus there are one or two small bright green fluorescent bodies. Plasmatocytes are irregularly shaped and their nuclei are invisible. Oenocytoids belong to the third group, and their nuclei are positive for propidium iodide. Therefore, all five types of circulating hemocytes of the silkworm, including many peculiar ones that are difficult to identify by light microscopy, can now be easily classified by fluorescence microscopy following staining with acridine orange and propidium iodide. In addition, we show that hemocytes positive for acridine orange and propidium iodide are in fact living cells based on assays for hemocyte composition, phagocytosis, and mitochondrial enzyme activity.

Acridine Orange↗
PubMed1991

Acridine orange as a probe for measuring pH gradients across membranes: mechanism and limitations.

Acridine orange is an optical probe commonly used to monitor pH gradients across membranes. In the present study, the changes observed in the visible absorption spectrum of acridine orange during intravesicular acidification of oat root plasma membrane vesicles are shown to be identical with those obtained by increasing the free dye concentration, adding anions, or lowering the temperature, but different from those obtained on addition of biological membranes. It is therefore suggested that the absorbance changes observed during the formation of the pH gradient are simply due to accumulation of free dye inside the vesicles and subsequent dimerization, and not the result of dye-membrane interactions. The proportion of monomeric acridine orange that could undergo dimerization decreased with decreasing temperature. Furthermore, in a membrane-free system different anions induced the formation of dimer-excimer complexes to different degrees. During the formation of the pH gradient permeant anions present in the reaction medium follow the movement of protons into the vesicles, and the intravesicular accumulation of anions thereby amplifies acridine orange quenching, the degree of amplification being dependent on the anion species. Therefore, the use of acridine orange, and probably all metachromatic dyes, as probes for monitoring pH gradients is limited, since these probes neither reflect quantitatively the amount of H+ pumped nor the effect of anions and temperature on transmembrane H+ transport.

Acridine Orange↗